Infection with EBV during infancy results in a lifelong latent infection of memory B cells, although not all EBV infections result in B-cell tumorigenesis. eBL is restricted to malaria-endemic regions of Africa, and acute malaria infection dramatically increases the levels of circulating EBV. According to earlier research published by the authors, the cysteine-rich inter-domain region 1-α (CIDR1α) of the highly expressed protein P. falciparum erythrocyte membrane protein 1 (PfEMP1) induces proliferation and activation of memory B cells. The latest report details the effects of CIDR1α on the reactivation of latent EBV in B cells.
Chêne et al. showed that red blood cells infected with P. falciparum, which express huge amounts of PfEMP1, and purified CIDR1α both bind to EBV-carrying B cells. Importantly, the binding of CIDR1α to EBV-carrying B cells resulted in a large increase in virus titre that could not be attributed to either increased apoptosis (leading to virus release) or B-cell proliferation. To directly show that CIDR1α stimulates reactivation of EBV from latency to a lytic replication cycle, the authors used a B-cell line that is a reporter for induction of the lytic replication EBV cycle through a fusion of green fluorescent protein (GFP) to an EBV lytic gene. They showed that the addition of CIDR1α results in the upregulation of GFP expression, with a concomitant increase in released EBV genomes that is consistent with reactivation of the EBV lytic replication cycle. CIDR1α had the same effect on EBV-carrying B cells from the tonsils of both healthy donors and those suffering from eBL.
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